Clinical
Considerations in Diagnosis of the Pathomechanical Temporomandibular Joint

Dennis
P. Steigerwald, D.C.
Wesley Shankland, II, D.D.S., M.S., Ph.D.

Temporomandibular
disorders (TMD) are a subclassification of musculoskeletal disorders (62,
63). Symptoms of TMD are associated with dysfunction of the craniomandibular
region. Tumors, vascular disorders, primary neurologic disorders and odontogenic
pains are not included under the heading of TMD. Rheumatologic disorders
which affect the temporomandibular joints include rheumatoid arthritis,
systemic lupus erythematosus, ankylosing spondylitis and psoriatic arthritis
(62). Local TMD symptoms include jaw pain, painful clicking in the temporomandibular
joints and limited capacity for mandibular function such as chewing and
mouth opening. Limitations in mandibular function are usually pain-mediated,
however mechanical limitations which the patient perceives as dysfunctional
are also considered local TMD symptoms. Other symptoms reported to be
produced by this region include, but are not limited to, neck pain, headache,
upper trapezius pain/stiffness, upper extremity pain/paresthesia, ear
pain, subjective hearing loss, dizziness and tinnitus (14, 33, 40, 62,
105, 106). It should be noted that a wide variety of rather obscure symptoms
have been attributed to TMD with little scientific work supporting a direct
relationship between tissues of the craniomandibular region and these
symptoms. Chronic pain has been associated with TMD, although a clear
etiologic relationship between psychological profile and TMD has not been
established (48). Research in the form of anesthetic injection studies
and retrospective surgical analyses have developed some statistically
supported statements that dysfunctional craniomandibular tissues can produce
symptoms at some distance from themselves including certain symptoms which
appear quite general in nature. It has been demonstrated for example that
headache, neck pain, upper shoulder muscle pain, dizziness and tinnitus
can be direct manifestations of the pathophysiology/pathomechanics of
the temporomandibular joints specifically (105). These findings may be
explained by the impact of the trigemino-cervical system on other cranial
nuclei (e.g. cranial XI), the cervical dorsal horn, the thalamus and higher
order brain centers. The extreme caudal extent of the spinal tract of
the trigeminal nerve is still under investigation (1).

TMD SYMPTOMS AND
SYMPTOM CHARACTERISTICS

1. The most common
symptoms of a temporomandibular disorder are:

Ear symptoms.

Headache.

Neck and upper
shoulder muscle pain.

Jaw pain.

Temporomandibular
joint noise (clicking, grating) with mandibular movement. (This is only
a symptom if it is painful or associated with dysfunction)

3. The most common
headache presentations associated with a temporomandibular disorder are
frontotemporal and suboccipital (109). It is not uncommon for a patient
to express the experience that the headache comes up from the neck to
the skull when the driving force behind the headache is in fact the inflammation
in the temporomandibular joints (105). If inflammation and/or derangement
of the temporomandibular joints is producing the headache, patients usually
experience these headaches at least two to three times per week if they
are not receiving treatment or are not placed on a home care program (109).
Less frequent experience of untreated headaches is more likely to be a
functional myofascial disorder or a headache which is unrelated to the
temporomandibular joints specifically.

4. When inflamed
temporomandibular joints produce neck and upper shoulder pain, this pain
is predominantly in the lateral cervical, upper trapezius and/or suboccipital
regions. This is not referred pain as the involved muscles will be hypertonic
and tender to palpation. It is very unusual for inflamed temporomandibular
joints to produce only posterior central cervical pain.

Research into the
pathomechanics and pathophysiology of TMD has been extensive (8, 25, 39,
52, 85, 87, 100) and parallels investigation of the dysfunctional and
symptomatic intervertebral joint motion segment closely. In both bodies
of research the biochemistry, architectural relationships, kinematics
and neurology of joints, muscles, tendons, discs and ligaments have been
investigated. All of these tissues have been implicated in various clinical
disorders. Recent interest in both fields has focused on the impact of
musculoskeletal pathology on the central nervous system and the complexities
of symptoms generated therein. Despite this rather large body of research,
clinical approaches to TMD still tend to be rather general and often are
based on unfounded or even disproved hypotheses.

The primary pathomechanics,
pathophysiology and neuropathology of the region are in fact often ignored
in the clinical setting. The primary areas of TMD investigation include:
the nature of TMD, etiologies of TMD, prevalence of TMD and the effects
of treatment on TMD. There are, of course, many other issues being investigated
concerning TMD, e.g. predictability, prevention and risk factors. This
parallels research on the symptomatic intervertebral joint motion segment
and other disorders of articular origin.

FUNCTIONAL ANATOMY

The temporomandibular
joint or craniomandibular articulation is a ginglymoid-arthrodial joint.
Each joint is an articulation between the articular tubercle eminence
of the squamous portion of the temporal bone (the mandibular fossa or
glenoid fossa) and the mandibular condyle. A fibrous disc, which acts
as a third bone, is interposed between the condyle and the fossa formed
by the temporal bone. These paired joints and the mandible, a single bone
that crosses the skeletal midline, function together since neither joint
is capable of independent movement. That is, one temporomandibular joint
cannot possibly move without producing movement in the opposite joint.

The human mandible
is the first bone of the body to demonstrate an ossification center. At
approximately six weeks in utero, developing from the mandibular process
of the first branchial arch, the mandible is seen as a thin plate of bone
in close association to the lateral side of the anterior region of Meckel's
cartilage on both sides of the developing face (24). Although Meckel's
cartilage does not contribute much to mandibular development, it does
to the incus, malleus, sphenomandibular and malleo-mandibular ligaments.
All major portions of the mandible (the body, ramus, coronoid and condylar
processes), develop by intramembranous ossification. Only the articular
surface of the condyle and the tip of the coronoid process develop by
endochondral ossification. The articular eminence of the temporal bone
is composed of compact bone overlying trabecular bone with marrow spaces.
Both the articular eminence and the articulating surface of the condyle
are covered with fibrocartilage, not hyaline cartilage, as in most other
articulations of the body.

The temporomandibular
joint is richly innervated by three different branches of the third division
of the trigeminal nerve (10). The auriculotemporal nerve, providing innervation
to the posterior, lateral and some medial portions of the joint, contributes
approximately 75% of the total sensory supply to the joint. Anterior and
medial innervation of the temporomandibular joints is provided by the
masseteric nerve, giving about 15% of the total innervation. The posterior
deep temporal nerve, supplying about 10% of the this innervation, furnishes
sensory innervation to a small area in the anterolateral portion of the
joint.

Blood flow to the
temporomandibular joints is also abundant and from many sources. The principle
blood supply comes from the superficial temporal artery and branches of
the maxillary artery, both of which are the terminal branches of the external
carotid artery. Venous drainage is provided by companion veins, all of
which contribute to the retromandibular vein, and by the facial vein,
which contributes to the anterior jugular vein.

ANATOMICAL CHARACTERISTICS
OF THE TEMPOROMANDIBULAR JOINTS

The temporomandibular
joints are synovial joints and share many characteristics common to all
synovial articulations (2). The temporomandibular joints exhibit several
anatomical features which are somewhat unique and delineate them from
other synovial joints, however. All synovial joints are weight or load
bearing and the temporomandibular joints are no exception. The following
structural characteristics contribute to the integrity and biomechanics
of this joint system.

ENCAPSULATION

To meet the demands
of the metabolism of the non-vascular articular surfaces of any synovial
joint, synovial fluid must be present at all times. Total enclosure or
encapsulation of such a joint allows for the containment of this fluid.
Each temporomandibular joint is confined within a fibrous capsule which
is attached superiorly to the articular eminence of the temporal bone,
posteriorly to the squamotympanic fissure and between these attachments
to the edges of the mandibular fossa, and inferiorly to the neck of the
mandibular condyle (37). The joint capsule is highly vascularized, well
innervated and lined with synovium. The synovium lines all aspects of
the joint that are not subject to load bearing. The capillaries in the
capsular walls engage in free metabolic exchange with the synovial fluid
within the joint. In addition, the synovial fluid provides lubrication
and phagocytic activity. The fluid is a dialysate of plasma and lymph,
consisting of a mucopolysaccharide complex (80) chiefly, hyaluronic acid.
The capsule is innervated by both free nerve endings and specialized receptors
(54, 69). Specialized receptors include Rufftni endings and Vater-Pacini
corpuscles. Free nerve endings (small, type III and IV) are the dominant
receptor type in the temporomandibular joints (108). Nerve endings are
not found on the load bearing surfaces of the temporomandibular joint
nor are they found in the articular disc except for mechanoreceptors at
the extremes of its periphery (69). Free nerve endings in the temporomandibular
joint serve as both mechanoreceptors and nociceptors (108). All receptors
have their cell bodies in the trigeminal ganglion and relay information
to the nuclei of the trigerninal nerve (10, 22, 28), the thalamus (74,
75) and higher brain centers (28).

ARTICULAR DISC

The temporomandibular
joint is classified as a compound joint. A compound joint, by definition,
requires the presence of at least three bones or surfaces (e.g. the capitulurn
and trochlea of the humerus articulating with the radius and ulna forming
the elbow). However, the articular disc interposed between the condyle
and mandibular fossa functions like a non-ossified third bone, thus forming
a compound joint. The articular disc of a temporomandibular joint articulates
superiorly with the articulating surface of the temporal bone and inferiorly
with the capitulum of the mandibular condyle. The disc is continuous on
its lateral and medial surfaces with the joint capsule, posteriorly with
the retrodiscal tissue, and anteriorly with the joint capsule and a small
portion of the superior head (approximately 2.4-6%) of the lateral pterygoid
muscle (5).

The disc is a true
disc. That is, a temporomandibular joint disc will divide the joint into
two separate compartments. This is in contrast to a meniscus (e.g. the
knee) which does not divide the joint, but extends freely into the joint
compartment and attaches to the capsule only by one edge (3). The space
between the disc and the temporal bone is called the superior joint space
or compartment and is anatomically discrete from the smaller, inferior
joint space between the disc and the condyle. Violation of this relationship
occurs when the disc or retrodiscal tissue becomes perforated. This allows
for direct contact of the bony articular surfaces and may or may not be
associated with symptoms. The superior joint space allows for translation
of the disc along the articulating temporal surface and the inferior joint
space accommodates rotation of the condyle under the disc. Pathomechanical
restriction of the capacity for gliding in the superior joint space has
been observed to be important clinically and will be discussed later in
this chapter. The disc is firm and biconcave in shape. It is comprised
of fibrous tissue which is organized in sheets of antero-posteriorly oriented
fibers on the superior and inferior surfaces, with thicker anterior and
posterior peripheral areas made up of fiber oriented in all three directions
and space (2). These fiber orientations provide for a most interesting
structural design which resists displacement of the disc bodily (anteriorly
and posteriorly) from the condyle during mandibular translation. Rees
(89) divided the articular disc into four sections:

The anterior band
which is a thickened anterior portion of the disc.

The intermediate
zone (or band), which is a narrow and thin area of the disc, interposed
between the anterior and posterior bands.

The posterior
band, which is a thickened posterior portion of the disc.

The bilaminar
zone (retrodiscal tissue).

These discal contours
provide joint stability by continual contact of all articulating surfaces
during joint motion. After the approximate age of 2 years the disc is
avascular and alymphatic depending on diffusion through the synovial fluid
for nourishment. This avascular condition is required as pressure on blood
vessels and nerves could not be tolerated. It was stated earlier that
the disc is continuous laterally and medially with the joint capsule.
However, it is more accurate to say that the disc is bound by firm attachments
directly to the condyle. The relationship of these attachments to the
capsule is an area of some debate.

RETRODISCAL TISSUE

The retrodiscal tissue,
also known as the bilaminar zone, is an area posterior to the articular
disc which is comprised of two separate layers or laminae. It extends
from the superior/posterior most portion of the posterior band of the
disc back to the tympanic plate and to the posterior aspect of the neck
of the mandibular condyle. This structure is folded in an accordion-like
fashion when the mandible is at rest or the teeth are in full contact
and is stretched and extended during protrusive and mouth opening movements.

The superior stratum
of the retrodiscal tissue, which is richly innervated by the auriculotemporal
nerve, is a very important structure in temporomandibular joint biomechanics
(121). This structure is often inappropriately referred to as a ligament.
It is actually composed of elastic connective tissue which produces a
passive posterior force on the articular disc during its forward movement.
This traction serves to rotate the disc in a posterior direction during
condylar translation (4). This arrangement adds to the stability of the
joint by keeping a firm contact between the articulating surfaces. Disc
movement is thus considered to be a function of disc shape and the collateral
attachments which tie the disc to the condyle. Any forward movement of
the articular disc during condylar translation is counteracted by elastin
fibers in the superior straturn. Elastin, an extracellular tissue fiber,
exhibits true elasticity (31). Injury, especially sudden injury to the
temporomandibular joints during the extension phase of whiplash can produce
an irreparable injury to these elastin fibers. Because elastin, unlike
collagen, does not have the capacity for repair, such injuries may allow
anteromedial displacement of the articular disc, especially if the lubricating
capacity of the synovial tissue is lost and adhesions develop which compromise
disc mobility. Following such anteromedial disc displacement the characteristic
clicking in the temporomandibular joints associated with internal derangement
may develop immediately or over time subject to these pathomechanical
forces (107, 117).

The inferior stratum
of the retrodiscal tissue is composed of loose areolar tissue made up
of chiefly non-elastic collagen fibers and possibly elastin as well (36).
This structure passively limits forward rotation of the disc on the condyle
during translation of the mandible.

Anterior to the superior
stratum but posterior to the condyle, is another vascular region termed
the vascular knee. This vascular area extends throughout the retrodiscal
tissues and contains numerous arteriovenous shunts. In this area, blood
is shunted in and out with mandibular function (94). When the mandible
translates forward, a negative pressure occurs in this area and when the
condyle moves back into its normal resting position in the mandibular
fossa, a positive pressure is produced. These pressure changes serve to
move synovial membranes within the joint compartments, thus producing
a near constant volume in the compartments during joint function. The
volume of synovial fluid cannot change as quickly as the mandible moves,
so therefore, the movement of blood into these arteriovenous shunts during
mandibular movement helps to maintain a constant joint pressure and moves
synovial fluid. In persons with a displaced articular disc, the compression
of this retrodiscal tissue between the condyle and articular eminence
of the temporal bone may or may not produce pain. It has been demonstrated
that this area is capable of metaplastic remodeling (53) and many persons
with anteriorly displaced discs do not experience pain (81). Pain is produced
when inflammation and adhesions activate nociceptors. Relatively rapid
disc displacement associated with inflammation is more likely to produce
retrodiscogenic pain than that which occurs gradually over years. The
importance of ideal disc position in a joint system which demonstrates
such extreme capacity for remodeling and repair remains an issue of scientific
and clinical debate to date (53).

ARTICULAR SURFACES

The bony components
of the temporomandibular joints are not covered with hyaline cartilage
(2). These articulating surfaces are instead covered by fibrocartilage,
which is a growth cartilage of a secondary type, not an articular cartilage.
This fibrocartilage is capable of extensive repair and remodeling, thus
resisting aging and anatomic breakdown (53). Specifically, the compact
bone of the condyles and glenoid fossae are covered by layers of cartilage
cells, mesenchymal tissue and fibrous tissue. While signs of degenerative
joint disease (DJD) are found in the human temporomandibular joints, it
is most frequently asymptomatic (47). This replacement of articular tissue
with lesser quality tissue is clinically and radiographically indistinguishable
from true remodeling (83) which is, by far, the more common process in
the human temporomandibular joint. Clinical expression of symptoms usually
follows a precipitating event such as trauma (47) and in that regard temporomandibular
joint DJD is not unlike other forms of DJD. Remodeling of the temporomandibular
joint articular surfaces has been associated with specific chemical mediators
(I-L and tumor necrosis factor (TNF)) (64). It should be noted that articular
cartilage is estrogen sensitive. In fibrous joints, such as the temporomandibular
joints, estrogen stimulating chemicals have been demonstrated to accelerate
DJD and estrogen repressors to slow the process (92). This may partially
explain the prevalence of females in most populations of TMD patients.
In fact, lower estrogen levels in post menopausal females may partially
explain why TMD is less common in the elderly population.

LIGAMENTS

The mandible is suspended
from the skull primarily by the temporomandibular ligaments or external
lateral ligaments (36). These ligaments suspend the mandible and resist
its posterior and superior displacement. Each ligament consists of two
distinct portions:

An outer oblique
portion which originates on the lateral surface of the articular tubercle
of the temporal bone and travels posteriorly and inferiorly inserting
into the outer lateral surface of the condylar neck.

An inner horizontal
portion which originates from the lateral portion of the articular tubercle
and travels posteriorly to insert into the lateral condylar pole and
articular disc.

The sphenomandibular
ligament is also known as the internal lateral ligament (37). Classically,
anatomy texts have listed its origin as the angular spine of the sphenoid
and the petrotympanic fissure. However, it actually is a combination of
the anterior malleolar ligament (79) which attaches to the anterior process
of the malleus. This small ligament passes through the pterygotympanic
fissure and the medial portion of the temporomandibular capsule and continues
as the sphenomandibular ligament inferiorly and slightly laterally insert
into the medial portion of the mandible. This ligament is passive during
mandibular movements and maintains approximately the same amount of tension
during opening and closing of the mouth (23).

The articular disc
is attached to the mandibular condyle by small and firm medial and collateral
attachments. While similar to ligaments, these structures are termed attachments
as they join a disc to a bone rather than a bone to a bone. Being intricately
involved with condylar motion these small structures limit the degree
of rotation of the disc on the condylar head and contribute to disc movement
during condylar translation. The lateral collateral attachment is the
most common to be stretched or torn with mandibular injury, thus permitting
anteromedial displacement of the articular disc which can result in clicking
or even locking of the temporomandibular joints.

The stylomandibular
ligament has been termed a specialized band of the cervical fascia in
anatomical texts. However, it has recently been demonstrated that this
structure is in fact a true ligament. This ligament serves to limit protrusive
movement of the mandible (101, 102). It originates from the styloid process
of the temporal bone and inserts into the medial aspect of the angle of
the mandible approximately 1 cm above the inferior border between the
masseter and medial pterygoid muscles.

MANDIBULAR MOVEMENT

The two basic mandibular
movements are translation, which takes place in the superior joint space,
and rotation which occurs in the inferior joint space. Rotation frequently
occurs along a shifting axis according to translational movements. These
joint actions occur during both empty mouth mandibular movements and masticatory
functions. All mandibular movements occur as a result of complex muscular
interactions controlled by even more complex integrated neural functions.
The integration of these movements is not completely understood. Pure
mandibular closure appears to involve the activation of muscle spindle
afferents and golgi-tendon organs at the junction of muscles and tendons
which excite, through monosynaptic reflexes, the alpha motor neurons of
the motor nucleus of the trigeminal nerve. The motor nucleus also receives
input from the cerebral cortex, the cerebellum, the reticular formation
and other cranial nerve nuclei (21). Motor axons leave the nucleus, projecting
out of the ventral pons via a small motor root that passes below the trigeminal
ganglion, join the mandibular division of the trigeminal nerve and are
distributed to the muscles of mastication (masseter, temporalis, medial
and lateral pterygoids) as well as the tensor veli palatini, tensor tympani,
anterior digastric and mylohyoid.

Mechanoreceptor afferents
provide input to the mesencephalic nucleus from receptors in the periodontal
tissues, tongue, palate, larynx and temporomandibular joints (20). These
same afferent fibers, projecting to the mesencephalic nucleus, also synapse
with cells within the motor nucleus. Therefore, jaw closure is a complex
series of afferent signals to the motor and mesencephalic nuclei producing
efferent activity in the muscles responsible for jaw closure. These muscles
include the masseter and temporalis primarily as well as the medial pterygoids.
The superior bellies of the lateral pterygoids also contract during closure
and contribute to joint stability.

The jaw opening reflex,
which is inhibitory to the jaw closure reflex, is mediated by the motor
nucleus of cranial V through the reticular formation (20). This inhibitory
reflex may also involve the spinal trigeminal tract, chiefly the pars
caudalis. There is little actually known about the neural integration
of these interactive opening and closing reflexes in humans. It is considered,
however, that since there are no temporomandibular joint articular receptors
which monitor loading, receptors in the periodontal ligaments and masticatory
muscles likely serve in this capacity (108). It is known that if the jaw
opening reflex dominates, then the anterior and posterior bellies of the
digastric, platysma, suprahyoids (chiefly the geniohyoid, mylohyoid and
stylohyoid) and inferior bellies of the lateral pterygoids are activated
to open the mouth. Further, the infrahyoid muscles (sternohyoid, omohyoid,
sternothyroid and thyrohyoid) fix the hyoid bone thereby assisting in
mouth opening.

Even less is understood
about the neuroanatomy of lateral movements of the mandible. It is known,
however, that lateral movements are accomplished by simultaneous contraction
of the contralateral medial pterygoid and inferior head of the lateral
pterygoid in concert with the ipsilateral temporalis posterior belly.
Protrusive mandibular movements represent a coordinated effort of the
inferior bellies of the lateral pterygoid muscles, the bilateral anterior
digastric muscles and the medial pterygoids.

JOINT MOTION

Until McNamara (61)
and later Mahan et al (55) demonstrated that the two bellies of the lateral
pterygoid muscle actually function independently and antagonistically,
temporomandibular joint motion was poorly understood. The inferior head
contracts upon mouth opening and the superior head contracts with closing
of the mouth. The larger inferior head originates from the lateral surface
of the lateral pterygoid plate of the sphenoid and inserts into the head
and neck of the condyle. When this muscle contracts along with the platysma,
digastrics and suprahyoid muscles, the condyle is pulled down and across
the articular eminence. Mouth opening is initiated by gravity, the relaxation
of the elevator muscles, contraction of the suprahyoid muscles and stabilization
of the hyoid by the infrahyoid muscles. This initial movement drops the
condyle down and away from the temporal bone and produces rotation of
the condyle within the fossa up to approximately 20 to 25 mm of mouth
opening. This is followed by contraction of the inferior heads of the
external pterygoid muscles which results in translation of the condyle
and intervening disc on the articular eminence. As the mandible is moved
forward the articular disc rotates posteriorly on the head of the condyle.
This posterior rotation is limited by the collateral attachments which
tie the disc to the medial and lateral poles of the mandibular condyle.
The disc then travels anteriorly with the condyle as the mouth opens to
maximum capacity. With this motion elastin fibers of the superior stratum
of the retrodiscal tissue stretch exerting posterior traction on the translating
disc. Throughout this entire mechanical activity a healthy articular disc
remains interposed between the condyle and the articular eminence.

When mouth closing
is initiated the inferior belly of the lateral pterygoid relaxes as the
superior head contracts. This superior head originates from the inferior
orbital rim of the sphenoid and inserts primarily into the pterygoid fovea
of the condyle. A substantially lesser portion attaches to the anteromedial
aspect of the capsule and to the articular disc. In a study by Bittar
et al (5) the percentage of the superior head which attached to the disc
was found to average approximately 2.4-6%. Contraction of the superior
head theoretically helps to stabilize condylar dynamics during mouth closure
and to some extent may influence disc position. Any substantial influence
on disc position seems unlikely, however. The disc then effectively rotates
forward as it translates posteriorly during the condyle's movement back
and up into the mandibular fossa. Optimum disc position during joint movement
is maintained then primarily by disc shape, although it is influenced
by the collateral attachments, the retrodiscal tissue and possibly somewhat
by the superior head of the external pterygoid musculature.

TEMPOROMANDIBULAR
DISORDERS

Temporomandibular
disorders have traditionally been subclassified as intracapsular and extracapsular.
Extracapsular diagnoses include myofascitis, myositis, myospasm and muscle
splinting. Coronoid tendinitis and Ernest syndrome are also included in
this category. Intracapsular disorders include capsulitis, synovitis,
retrodiscitis, symptomatic disc displacement (with or without reduction),
disc/retrodiscal perforation, ankylosis and symptomatic hypermobility
(including joint dislocation). There is no specific lesion or pathology
implied under the general heading of TMD, nor are there definitive symptom
presentations. Many symptoms have been attributed to both intracapsular
(105) and extracapsular (112) disorders yet acceptable inclusionary and
exclusionary factors for some subsets of TMD are still lacking. Difficult
questions have in fact been raised concerning the clinician's ability
to distinguish primary myofascial TMD from arthrogenous temporomandibular
joint disorders (105).

*Muscle splinting
is a muscular response to pathology which may be initiated by intracapsular
or extracapsular nociceptive events.

EXTRACAPSULAR
DISORDERS

Primary myositis
and myospasm are rather rare clinical entities. Myositis presents as an
acute continuous muscular pain usually following infection or trauma.
The muscle will be swollen and warm to the touch. Pain-mediated limited
range of motion will be specific to the involved muscle(s). Myospasm has
a similar presentation, although the muscle will not be as warm to the
touch or swollen. During myospasm the muscle(s) is fully contracted even
at rest. Limited mandibular range of motion is pain-mediated and specific
to the involved muscle(s).

When an extracapsular
TMD is suspected, a myofascial diagnosis is by far the most common made.
Masticatory myofascitis has the following characteristics:

Tender points
and/or trigger points are found in the involved muscles.

Patients present
with cyclic, dull, local aching pain.

In uncomplicated
myofascitis mandibular range of motion is not restricted.

It has been hypothesized
that myofascitis has many potential etiologies. These include postural
overload, mechanical overload, injury, elevated sympathetic activity (local
or systemic) and joint, tendon and/or ligament inflammation-mediated central
excitation. While masticatory myofascitis is thought to occur in a manner
similar to that proposed for other muscle systems then, in the masticatory
system muscle overload is thought to occur as a result of oro-facial parafunctional
habits or extremely vigorous chewing. These parafunctional habits include
lip biting, thumb sucking, fingernail biting and especially bruxism (63).

Bruxism consists
of two activities which may be present in the same patient or which may
occur separately. These activities include clenching the teeth together
and grinding the tooth surfaces over each other. Clenching and/or grinding
of the teeth may occur while the person is awake and/or during sleep (76).
Bruxing while awake is most often considered a reaction to stress and
may represent a manifestation of elevated sympathetic activity. Nocturnal
clenching/grinding of the teeth may be a stress reaction (123) or may
represent a manifestation of a primary central nervous system disorder
or sleep disorder (88). Despite clinical acceptance of bruxism as an an
etiology of TMD, it should be noted that Pullinger et al (86) found no
association between tooth grinding as measured by tooth attrition and
TMD except for myalgia in young males. It is interesting to note that
in contrast to myositis and myospasm, which follow a clear precipitating
event, masticatory myofascitis is usually cyclic (90) with no clear single
etiology. Proposed etiologies such as malocclusion and bruxism have been
observed to be equally prevalent in the TMD population and in the general
population (18, 20, 34, 78, 84, 97, 98). It appears that cyclic expression
of masticatory myofascitis may be a local expression of a systemic increase
in sympathetic activity, the effects of which may vary according to the
occlusal architecture and parafunctions specific to the individual. The
implications of this are profound in terms of whether to treat a patient
for a cyclic myofascial disorder and, if treatment is proposed, how best
to go about it. Stress management and biofeedback often play a role in
treatment of primary myofascitis as may management of sleep disorders
(123). Intermittent use of oral orthotics (65, 120) as well as palliative
physiotherapy applications (6) have been recommended. It should be noted
that if muscles are not injured, they should relax in a relatively short
time (within one to two days) if the stimulus for hypercontraction is
removed. This principle should guide diagnoses and treatment of myofascitis.
It has been suggested that sustained local symptoms of muscle hyperactivity
may indicate the presence of an intramuscular inflammatory response (123).
Marcel et al (58) demonstrated biochemical changes in the muscles of frequent
bruxers and this data May be productive in future research of this phenomenon.

Non-muscular extracapsular
TMDs include coronoid tendinitis (29) and Ernest syndrome (102, 103).
These disorders involve inflammation of the temporal tendon(s) and stylomandibular
ligament(s) respectively. The most common cause of both disorders is trauma
especially that associated with rapid, prolonged and/or excessive mouth
opening. The symptoms of temporal tendinitis (coronoid tendinitis) include
both local pain (usually with attempts at mouth opening) and symptoms
expressed at a distance from the inflamed tissue. These symptoms include
temporomandibular joint pain, ear pain and pressure, posterior maxillary
tooth pain, ipsilateral eye pain and temporal headache with extension
to the occipital, posterior auricular and cervical regions. The temporalis
coronoid attachment will be tender to intraoral palpation when it is inflamed.
This tenderness is often mistaken for tenderness of the inaccessible external
pterygoid. Reproduction of the patient's symptoms with palpation supports
this diagnostic impression and elimination of symptoms with anesthetic
injection confirms the diagnosis. It is not surprising that the symptoms
of temporal tendinitis are similar to those of a primary temporomandibular
joint intracapsular inflammation as they share the neurology of the deep
temporal nerve (101). Temporal tendinitis can be found in conjunction
with or separate from temporomandibular joint inflammation and differential
diagnosis requires a thorough examination of the temporomandibular joint
complex. While inflammation of the temporomandibular joint may cause coronoid
tendon tenderness secondary to sensitization of the deep temporal nerve,
the reverse is not commonly observed. In complex and resistant cases anesthetic
injection often provides the most accurate diagnostic insight.

Ernest syndrome is
an inflammatory disorder of the stylomandibular ligament (103). Symptoms
are similar to temporal tendinitis except that mouth opening will not
produce pain at the coronoid process and throat pain may be present. A
diagnostic impression is developed by history, location of tenderness
and symptom reproducibility during palpation. Diagnosis once again is
confirmed by anesthetic injection.

Muscle splinting,
while usually listed under extracapsular disorders, is a unique phenomenon.
The diagnosis of muscle splinting implies a protective muscular response
to pathology (122) which may be intracapsular (e.g. synovitis) or extracapsular
(e.g. temporal tendinitis). The characteristic signs and symptoms of masticatory
muscle splinting are limited range of motion which is specific to the
protected region, pain with mandibular movement (primarily mouth opening)
with little or no muscular pain at rest and a sense of weakness and/or
fatigue in the involved muscles. Muscle splinting is frequently mistaken
for a primary muscular disorder because of these signs and symptoms. If
muscle splinting is present, the primary pathology stimulating splinting
should be identifiable. The primary focus of irritation is usually capsular/
intracapsular inflammation, coronoid tendinitis or muscle injury. Primary
myofascitis will not cause muscle splinting. It should be noted that muscle
splinting will much more dramatically limit mouth opening than protrusive
or lateral mandibular movements.

INTRACAPSULAR
DISORDERS

The terms intracapsular
and arthrogenous when applied to TMD indicate that the driving force behind
the expression of symptoms is found within the temporomandibular joints
proper. While it has been understood for decades that pathologic changes
within the temporomandibular joints could result in local symptoms (119),
debate has continued over what association, if any, intracapsular disorders
have with myofascial presentations and other symptoms expressed at some
distance from the joints themselves. One school of thought holds that
intracapsular disorders are a subclassification of TMD separate from,
however related to, masticatory myofascitis and other muscular influences.
Research by Vallerand and Hall (113), Montgomery et al (68), Danzig et
al (17), Mosby (70) and Steigerwald et al (105) indicates that temporomandibular
joint pathology may in fact produce reactive myofascial presentations
in the head, neck and shoulder musculature as well as other symptoms including
dizziness, tinnitus and hearing loss (14). The reactive muscular component
will demonstrate hypertonicity and tenderness and may well produce tertiary
sites of pain when trigger points are produced and/or activated in the
involved muscles. This trigeminal affect on the cervical region was also
noted by Miralles et al (67) relative to the influence of stabilizing
oral orthotics on the sternocleidomastoid musculature. Variations in jaw
posture have also been observed to effect the sternocleidomastoid and
upper trapezial musculature (124).

The temporomandibular
joints are ideally constructed for adaptation, remodeling and repair.
Theoretically, this is necessary as this joint system is arguably one
of the most active and complex in the body and must adapt to shifting
occlusal, postural, functional and parafunctional influences over the
lifetime of the individual. Symptoms of the joint-specific intracapsular
or arthrogenous TMD may be confined to the joint system or demonstrate
complex neuro-myogenous referral patterns. Symptoms of arthrogenous TMD
develop when inflammation and biochemical degradation within the joint
exceed the capacity for repair (100) and/or when adhesions form within
the joints interfering with disc and/or joint mobility (71). Degenerative
joint disease (DJD) is defined as replacement of normal articular tissues
with tissue of lesser quality (47). While this has been observed in human
temporomandibular joints, it is observed in both symptomatic and no symptomatic
joints and does not identify a specific clinical entity (47). DJD of the
temporomandibular joints does not have a specific etiology and the temporomandibular
joints have not demonstrated a tendency toward progressive deterioration
and symptom expression. The only component of the temporomandibular joints
that has been histological observed to degenerate rather than remodel
when the disc is displaced is the disc itself (53).

SENSITIZATION
OF NOCICEPTORS IN THE TEMPOROMANDIBULAR JOINTS

Small (group III
and IV) receptors are the most numerous receptors in the human temporomandibular
joint (49). These fibers are sensitized by inflammation and mechanical
deformation such as capsular swelling (108). This decrease in the neural
threshold of stimulation may result in neural firing in response to what
would otherwise be considered non-noxious stimulation (15, 95). This may
explain why patients with articular driven disorders tend to have rather
constant symptom expression with fluctuations in intensity when compared
with primary myofascial disorders which tend to be truly cyclic. If nociceptors
within the temporomandibular joints are stimulated, pain may be experienced
locally and/ or along other pathways of the trigeminal nerve (137). Capsular
swelling and/or deformation may sensitize mechanoreceptors as well and
flood the trigeminal system leading to central sensitization and neuroplasticity
(99, 114). This may result in stimulation of other components of what
is referred to as the trigemino-cervical complex which includes cranial
nerves V, VII, IX, X, XI and XII as well as cervical nerves I through
IV (56). This can result in a diffuse spread of symptoms according to
the complexity of this system and its interaction with higher level CNS
centers. One of the results of this process appears to be elevated activity
of the sympathetic nervous system. Research by Hubbard et al (43) has
indicated that elevated sympathetic activity, whether local or systemic,
may affect the spindle cells of the muscles causing trigger point activation,
muscle shortening and local muscle tenderness. Muscles which can be affected
by this process include the masticatory muscles (9,30) as well as the
intrinsic cervical muscles, the sternocleidomastoideus and upper trapezius
(70,105). The reactions and symptoms of the neck and shoulder muscles
may be ipsilateral, contralateral or bilateral to the involved joint.
This was demonstrated clearly by Danzig et al (17) who investigated the
impact of anesthetic injected into symptomatic temporomandibular joints
on muscles of the neck and upper shoulder region. It is interesting to
note that in Mosby's study (70) it was observed that muscular response
to temporomandibular joint pathology was greater in the sternocleidomastoid,
upper trapezial and cervical musculature than in the masticatory muscles.

THE NEURAL ANATOMICAL
BASIS FOR MUSCULAR CO-CONTRACTION AND REFERRED PAIN IN ARTHROGENOUS TMD

To fully appreciate
the impact of pathomechanical and pathophysiologic influences on symptom
expression beyond the experience of local temporomandibular joint pain,
one must consider the central connections of the joint receptors. The
nucleus caudalis of the trigeminal system receives nociceptive input from
the oro-facial region (10, 38). This nucleus extends down to at least
the level of C3 in the spinal cord and convergence from cervical nerves
influences this region (7). Interneurons in this region relay information
to higher order centers as well as to other cranial nuclei (21). This
area may become sensitized as a result of temporomandibular joint-specific
neural influences (99, 114). Bradykinin and substance P spillover may
then influence regional cervical nerves and stimulate reactions in the
associated cranial nuclei and there higher order centers. The most likely
cranial nuclei to be affected include CR VII, IX, X and XI (124) as well
as other regions of cranial V including its motor nucleus (9, 99). This
process of joint receptor sensitization leading to interneuronal activation
with subsequent sensitization and neuro-plastic central reactions may
explain the plethora of symptoms peripheral to the temporomandibular joint
primary pathology. This includes myofascial presentations of the masticatory
and cervical regions which are often clinically mistaken for primary processes.
Another frequently misinterpreted symptom is masticatory muscle splinting
which can occur secondary to joint pathology (122). The clinical implications
of such misinterpretation cannot be overstated.

It is a well accepted
principle that the site of pain and the source of pain are different in
many disorders (77). The classic example of this is causalgic pain experienced
in a missing limb. Trigger point pain also represents a condition which
presents with the pain site separate from the pain source (111). These
complex clinical entities cause substantial diagnostic difficulties. There
are, however, clinical signs which aid in exposing the source of pain.
Trigger points for example will produce a typical pain pattern when they
are aggressively palpated and/or stretched. The area of pain, if it is
truly produced by a trigger point, will be non-tender unless there is
some other local pathology or tissue reaction present. Trigger point pain
is classically reduced or eliminated with anesthetic injection at the
source of pain while injection of the site of referred pain does not impact
the pain presentation (77). The most common peripheral symptoms produced
by temporomandibular joint pathology result from neural stimulation of
muscle activity which produces hypertonic and tender muscles (105). This
includes the masticatory and/or cervico-trapezial regions. Trigger points
may then arise from these affected muscles producing tertiary locations
of pain expression or other symptoms including dizziness and tinnitus.
The site of referred pain and the source of pain may thus become even
more obscured as the trigger points which now appear as the source of
pain are actually second level pain initiators activated by muscular response
to the primary joint pathology.

Symptoms local to
the dysfunctional temporomandibular joints include temporomandibular joint
pain, painful clicking in the temporomandibular joints and limited capacity
for mandibular movement beyond the tolerance of the patient (42). Local
symptoms of temporomandibular joint pathomechanics are just that ... symptoms.
That is, there must be some noxious experience reported by the patient
or some restriction in desired capacity for mandibular function for a
disorder to be present. There are no signs of joint dysfunction which
are predictive of symptom expression except in their extremes. This includes
clicking and other temporomandibular joint noises, deflection and/or deviation
of mandibular movement from the midline and less than optimal mandibular
range of motion. All of these findings are present in the patient and
non-patient populations studied and despite theories to the contrary,
none are predictive of eventual expression of pain or limited mandibular
capacity (19). The findings of temporomandibular joint noise, altered
mandibular tracking and/or limited mandibular range of motion do not constitute
symptoms and do not indicate the presence of a temporomandibular disorder
unless they are specifically noxious to the patient or are associated
with symptoms for which the patient is seeking care and which are traceable
back to the region.

TMD EXAMINATION

The examination of
this region involves six component procedures. Many portions of the examination
are integral to evaluation of any synovial joint system. However, the
craniomandibular region also has characteristics which are unique and
require special investigation.

The six parts of
the TMD examination include:

Case history.

Range of motion.

Mandibular tracking.

Palpation.

Auscultation.

Joint/muscle challenges
(provocations).

CASE HISTORY

Without question
the most important aspect of the clinical TMD examination is the case
history as this will establish the background against which clinical findings
can be interpreted. This is true of all musculoskeletal disorders. The
case history will help the clinician to decide if a TMD is present and
if so will help to answer questions concerning etiology and perpetuating
factors which may interfere with successful case management. In taking
the case history one should keep in mind that the etiologies of TMD remain
in question.

Trauma has been clearly
established as a precipitating factor for TMD (82, 85). There are two
types of overt trauma which are known to precipitate a TMD. The first
is direct trauma such as a blow to the mandible (35, 42). The second type
is indirect trauma usually associated with a "whiplash injury" (8, 11,
16, 27, 32, 35, 41, 50, 51, 57, 91, 93, 96, 104, 116, 117). Indirect trauma
has also been associated with protracted and/or excessive mouth opening
(35) such as may occur during oral intubation, a prolonged dental visit
or third molar extraction. When a clear precipitating event such as trauma
does not predate the onset of a TMD, other historical data which may shed
light on a possible etiology should be investigated such as: dental history,
orthodontic history, prior traumas, rheumatologic and medical history,
family history and parafunctions such as bruxism.

Mouth opening.
Mouth opening is generally considered normal at 40 to 50 mm. This should
be an unstrained vertical movement and is measured from the lower edge
of the upper central incisors to the upper edge of the lower central
incisors. If overbite (vertical incisal overlap) exceeds 1 to 2 mm add
the excess to the overall measurement.

Lateral mandibular
movement or laterotrusion is measured from maxillo-mandibular midline
(allowing for asymmetry) to the extreme of both right and left lateral
mandibular movement. The mouth is slightly open so that the teeth do
not touch during this test. This movement should be unstrained and should
not require an excess of mouth opening. Normal range is 10 to 12 mm
to each side.

Protrusion (forward
movement): The mandible can normally be protruded 10 to 12 mm from the
point of maximum occlusal contact. This should not require an excess
of mouth opening. It should be noted that during protrusive, as with
lateral movements, the mouth is slightly opened to avoid tooth-to-tooth
contact.

Patients who demonstrate
restricted ranges of motion which are mechanical in nature should prompt
a referral to a specialist in the treatment of temporomandibular disorders
especially if the onset is sudden and/or follows trauma. Restricted range
of motion is a complex affair and may be a sign of such disorders as disc
dislocation accompanied by ligament damage, muscle splinting, ankylosis
and/or frank myospasm. If a restricted active range of motion is noted,
an attempt may be made to assist movement manually. This is known as assisted
active range of motion. Active assisted range of motion may be coupled
with proprioceptive neuromuscular facilitation (p.n.f.) techniques to
minimize neuromuscular restriction. This is accomplished by having the
patient contract the restricting muscle against resistance and then subsequently
attempting movement with manual assistance in the desired direction. This
technique can be used for all three mandibular movements, but is most
commonly used to test restricted mouth opening. This test should be performed
gently and carefully.

Restricted range
of motion may be pain and/or mechanically mediated. Restricted movement
that is muscular/neuromuscular in origin may be temporarily modified with
p.n.f , massage and physiotherapy. Mechanical restriction (disc, adhesion,
ankylosis) is minimally modifiable, if at all, with musculoskeletal therapy.
Pain-mediated restriction may indicate muscle splinting secondary to primary
tissue inflammation. Differentiating primary muscle disorders from muscle
reactions to joint pathology is a critical step in the diagnostic process.
Misinterpretation can lead to misdirected treatment.

While there are no
range of motion limitations which enable the doctor to make an absolute
diagnosis, there are guidelines. The following should help you to develop
a diagnostic index of suspicion.

If mouth opening
is limited at 26 to 32 mm and not modifiable, one should suspect disc
dislocation (disc displacement without reduction). In this case protrusion
will be limited at approximately 4 to 8 mm. If the disc(s) are also
medially dislocated, laterotrusion (side-to-side movement) will be limited
to the side opposite the involved disc at approximately 4 to 8 mm. Other
causes of non-modifiable limited mandibular movement include joint ankylosis
which may be fibrous or bony and hypertrophy of the coronoid processes.
Limitations produced by these pathologies are frequently more extreme
than disc dislocation.

Limited mouth opening
with full protrusion indicates a neuromuscular/muscular problem (see palpation
exam for differential). The mechanical processes of ankylosis and/or coronoid
hypertrophy will limit movement in all directions specific to the involved
joint(s) and will be entirely non-modifiable with physical techniques
(manipulation, physiotherapy, massage). Keep in mind that with restrictions
below 25 mm you cannot know if the discs are displaced/dislocated because
they cannot limit condyle movement until that point. Disc dislocation
(displacement without reduction) will more profoundly affect protrusion
than opening. Limited mouth opening with normal protrusion is almost never
a disc-mediated phenomenon.

MANDIBULAR TRACKING

Ideal mouth opening
should be unstrained and appear as a vertical movement with no deviation/deflection
from the midline. Attempts at protrusive movement should, as well, be
unstrained and free from any lateral movement from the vertical midline.
Attempts at lateral movement should be unstrained and free from attempts
on the part of the patient to open the mouth in order to achieve lateral
movement.

Deviation is defined
as movement of the mandible away from the midline during opening and/or
protrusion without return to center during the movement. Deflection is
defined as movement of the mandible away from midline followed by a return
to center. As with limited range of motion deviation and deflection may
be the result of muscular, neuromuscular or mechanical factors. As previously
stated, muscular/neuromuscular influences may be modified with massage,
physiotherapy and p.n.f , while mechanical factors are minimally modifiable
and produce more of a repetitive, identical or similar pattern.

Joint mediated deviation
may indicate disc dislocation (anterior/medial), capsular adhesion or
ankylosis. The deviation will occur to the side of the pathology ("the
chin will point to the problem"). Deviation to the same side during mouth
opening and protrusion is virtually pathognomonic of a mechanical dysfunction
on the side of the deviation.

Mandibular deviation
has been documented in the nonsymptomatic population (39). Incidental
findings of mandibular deviation without related symptoms (local or peripheral)
are generally monitored rather than treated. If this finding arises or
develops during the continuum of symptoms following trauma and is associated
with limited opening and protrusion, it signals the possibility of a serious
joint pathology/injury. This condition is unlikely to remit spontaneously
and very well may fail conservative management. A second opinion with
an oral and maxillofacial surgeon is suggested for temporomandibular joint
injury when symptoms are coupled with mandibular deviation and/or signs
of locking. This is especially important now that minimally invasive arthroscopic
surgical techniques are available and have proven to be effective for
these conditions (42, 68, 71, 105). The more aggressive surgical intervention
of arthrotomy has also been shown to be effective for advanced therapy
resistant joint-specific disorders (119).

Mandibular deflection
may result from disc displacement with reduction and/or muscular influences.
Disc displacement may or may not be accompanied by adhesive restriction
of disc mobility. The more repetitive and non-modifiable the deflection
pattern the more likely that it results from disc displacement and that
the disc is adhesively restricted and possibly morphologically altered.
This condition may be unilateral or bilateral.

Two basic deflection
patterns are seen. The first is termed a "C" type deflection and indicates
a unilateral disc displacement on the side of deflection. This would indicate
that while the disc is displaced forward of the condyle and may be adhesively
restricted from translation in the superior joint space, it is not folded
or dysmorphic enough to prevent full condylar translation. During mouth
opening the chin will move to the side of the displacement and then return
to center. The other major deflection pattern is termed an "S" or "Z"
type of deflection indicating a bilateral displacement. This type of deflection
pattern occurs when both discs are displaced forward, one more than the
other (the second deflection indicates the more anteriorly displaced disc).
If both discs are equally dislocated or displaced there may be no deviation
or deflection, but rather limited mouth opening at 26 to 32 mm of opening
(bilateral disc dislocation) or simultaneous clicking/popping in the temporomandibular
joints bilaterally (bilateral disc displacement).

Deflections are frequently
associated with joint noises such as clicking/popping in the temporomandibular
joints. The noise will usually occur at the apex of the deflection on
the side of the displaced disc. It should be kept in mind that the disc
may be ideally positioned (not displaced), but adhesively restricted.
This can result in altered disc dynamics with deflection toward and clicking/
popping in the involved joint. In cases where clicking and deflection
are caused by joint pathology other than disc displacement, conflict between
clinical exam findings and an MRI of the joint(s) may result. (See special
tests section).

AUSCULTATION

Temporomandibular
joint noises were once considered almost pathognomonic of temporomandibular
disorders. New thought has led us to believe, however, that many joint
noises present with mandibular movement may be part of the natural history
of asymptomatic joints (83). These noises may be the result of remodeling
and accommodation processes which take place over time or the result of
specific architectural predispositions such as superior/posterior condyle
positioning. Clicking in the temporomandibular joints has been identified
in greater than 40% of the asymptomatic population (39). Any joint noises
arising or increasing within three months of trauma, such as whiplash,
and/or which are associated with continuing symptoms should be considered
important (107). Joint noises do not identify the presence of a temporomandibular
disorder, but help to classify the type of disorder when symptoms are
present (52).

Auscultation of the
temporomandibular joints can be performed with light digital palpation
or use of a stethoscope. Joint vibration analysis (JVA) machines are sometimes
used to record joint noises. These machines can accurately record many
characteristics of temporomandibular joint noises (45, 46). The data gained
from JVA needs to be interpreted in light of the history and entire clinical
exam however before an accurate diagnosis can be made.

During the standard
TMD examination the doctor should place the stethoscope and/or the finger
tips of the second and third digits lightly over the lateral poles of
the temporomandibular joints. This contact should be no heavier than light
skin contact to preclude putting pressure on the lateral poles of these
joints. The doctor instructs the patient to fully open and then close
the mouth. The patient is then subsequently instructed to protrude, retrude
and laterotrude the mandible. Various joint noises may be heard and should
be recorded. Joint noises are usually referred to as clicking, popping
and crepitus. Clicking/popping in the temporomandibular joints which occurs
within the normal range of motion (less than 40 to 50 mm) most frequently
occurs as a result of disc displacement and/or adhesions. This second
cause (adhesions) is important to remember because it clinically mimics
disc displacement, but may be interpreted as a normal joint on an MRI
(see special tests). Persistent joint noise coupled with continued symptoms
and joint tenderness is an important clinical finding whether it results
from disc displacement or adhesions. Clicking/popping in the temporomandibular
joints is often thought to occur as a result of "spasm" or incoordination
of the superior heads of the external pterygoids. This is very unlikely
however as research has shown that this muscle has little or no mechanical
advantage over the disc (5). Intermittent clicking which seems stress/clenching
related is more likely due to hypertonicity of the elevator muscles during
joint movements. The strong possibility of concurrent disc complex instability,
adhesions and/or disc displacement exists in these cases.

You may notice that
deflection is present without clicking during the examination. While this
may be a muscular affect, you should challenge this finding by modifying
your examination procedure. To do this, lightly grasp the chin and guide
the mandible through a straighter course of opening and protrusion. Muscular
influences on deflection are minimized then and clicking/popping and even
intermittent locking may be observed.

Clicking and deflection
are usually coordinated manifestations of the same event, i.e. discal
and/or adhesive interference with condylar translation. As such, uncomplicated
clicking usually occurs at the apex of mandibular deflection toward the
involved joint. Variations on this theme may occur, however. The most
important of these is encountered when deviation to one side is accompanied
by clicking on the opposite side. The doctor may misinterpret this clicking
as indicative of the primary problem, especially as this may be the more
painful side. It is the side toward which the mandible deviates which
is more profoundly deranged, however, especially if deviation occurs during
both protrusion and mouth opening lack of treatment of the side toward
which the mandible deviates will undermine any attempt to treat the side
productive of the clicking.

Crepitus may be detected
during auscultation. This is described as a "ground glass" sound and signals
the possibility of discal or, more commonly, retrodiscal perforation (43).
If this is present in a symptomatic joint, it identifies an advanced problem
which may prove difficult to manage even with surgical techniques. While
conservative care is appropriate and may prove successful, early referral
for surgical consultation is recommended if clear and steady progress
is not achieved. Crepitus may or may not be associated with deflection,
deviation and/or decreased range of motion. As with clicking, crepitus
may be present without symptoms if there is no associated inflammation.
These cases are generally monitored rather than treated unless there is
a report of shift in facial contour or occlusion. If alteration of facial
contour and/or a shift in occlusion is reported by the patient, they should
always be referred for an expert opinion.

Noises described
as popping or clunking may occur at the widest point of mouth opening
(generally 50+mm). These sounds occur as the condyle passes over the temporal
eminence. This indicates joint hypermobility. This may be a manifestation
of general ligament laxity or of local ligament damage/degradation. This
hypermobility is clinically more significant if the temporal eminence
is steep (like a vertical wall). Temporomandibular joint hypermobility
has been observed in the asymptomatic population. Coupled with symptoms
however it calls for strict patient compliance with instructions to limit
full mouth opening. If hyper-translation is allowed to continue after
inflammation has begun, substantial joint damage and even non-reducing
joint dislocation may occur as pathology progresses.

As a final point
in this section the issue of the "posterior disc" should be addressed.
This was a popular concept before accurate imaging techniques alerted
us to the prevalence of the anterior/medial disc displacement. As it turns
out the posterior disc is a very uncommon occurrence and when it is observed
it is usually a transient position which occurs during functional mandibular
movements. That is, if the disc is prevented from translating by adhesions
in the superior joint space, the condyle may click onto and past the disc
causing a momentary posterior disc positioning. In these cases generally
the closing click is louder than the opening click. This finding implies
that not only is the disc non-mobile, but that the collateral attachments
of the disc to the condyle are weakened allowing the condyle to move both
forward of and posterior to the disc during these respective condylar
movements. In contrast to this, the anteriorly displaced disc that is
not adhesively restricted and has intact collateral attachments presents
almost invariably with an opening click that is louder than the closing
click (the closing click may in fact be inaudible). The dysfunctional
posterior disc phenomenon may also occur secondary to changes in disc
shape. In our experience patients presenting with a dominant closing click
have a poor prognosis for success with conservative care. While conservative
care may be tried and very well may succeed, there is no scenario in which
thrusting the mandible in an A-P direction to seat the condyle under a
posterior disc is appropriate.

PALPATION

Palpation is perhaps
the most undervalued and misunderstood of the TMD exam procedures. Palpation
findings for muscles, joints, ligaments and tendons are often considered
equally reliable or unreliable and lumped under the heading of "subjective"
data. In fact, with regards to muscles and joints, inter-examiner and
serial intra-examiner reliability is different for each tissue. This includes
studies of the cervical, lumbar and masticatory regions (19, 44, 60,90).

The effectiveness
of palpation for differentiating patients from non-patients has not been
thoroughly validated. The following statements represent the reliable
information derived from skilled palpation:

Cervical and/or
masticatory muscle tenderness is not a reliable indicator of local muscle
pathology as tenderness may represent the affect of a CNS process stimulated
by peripheral pathology (90, 105, 115).

Identification
of trigger points by palpation is reliable (111).

In a patient population
tenderness over the lateral poles of the condyles identifies capsular
inflammation accurately especially if the tenderness is equal to or
greater than 2 on a 0 to 3 scale and the condyles are as tender or more
tender than the ipsilateral masseter and temporalis musculature (105).

Palpation of the
lateral and posterior capsule of the temporomandibular joint with an
algometer shows acceptable inter and intra-examiner reliability and
can identify patients from non-patients (13).

Many difficult questions
are now being asked which challenge our ideas about myofascial disorders.
In the field of TMD this is very troublesome as a "myofascial" diagnosis
is one of the most commonly assigned in clinical practice. Results from
four surgical studies and two temporomandibular joint anesthetic injection
studies challenge the idea that we can identify myogenous disorders exclusively
by the presence of muscular tenderness to palpation. These studies have
demonstrated remission of both masticatory and cervical myofascial tenderness
when the temporomandibular joints are injected with an anesthetic and/or
operated (17, 68, 70, 105, 113). This is not to say that all myofascial
presentations are driven by joint inflammation, but rather that muscle
tenderness alone cannot rule in a true primary myogenous disorder, cannot
rule out an arthrogenous disorder and cannot rule in a mixed arthrogenous/
myogenous disorder as the arthrogenous disorder is capable of driving
the entire muscular component (105). Joint tenderness as an isolated finding
may not be an accurate inclusionary factor for symptomatic capsulitis
as it has been noted that joint receptor discharge increases with muscle
activity (66). In fact, comparing locations, patterns and relative degrees
of tenderness in the muscles and joints of the head and neck may give
us the most useful diagnostic impression (105). It should be noted that
the presence of cervical muscle tenderness in patients expressing symptoms
in the head and neck has been identified as indicating a high probability
of TMD (40, 109, 115).

Palpation of the
masticatory and cervical/upper shoulder regions is necessary and important
in the TMD examination. These tests are necessary to satisfy the demands
of standard of care and can provide useful information in the following
ways. First, identification of trigger points and muscle hypertonicity
provides targets for treatment in true non-arthrogenous myofascial conditions
(112). Second, certain patterns of muscle tenderness and hypertonicity
can be informative diagnostically when temporomandibular joint tenderness
is present concurrently (105). Third, when temporomandibular joint pathology
is suspected of being the driving force behind the symptoms, specific
areas of muscle tenderness and hypertonicity can serve as target areas
for anesthetic temporomandibular joint injections and/or joint-specific
treatment trials (17, 105, 107).

TEMPOROMANDIBULAR
JOINT PALPATION - TECHNIQUE

To palpate the
temporomandibular joints most effectively have the patient move the
chin to the side opposite the joint palpated. When the joint is palpated
with the teeth together or the mandible at rest there is approximately
5-10 min of tissue between your finger and the joint capsule. Having
the patient maneuver the chin to the opposite side will surface the
condyle for more accurate palpation.

Palpate the condyle
with three to five pounds of pressure.

Palpate the entire
condyle accessible to you as the lateral capsule is complex and certain
areas may be tender while others remain nontender. Any tender areas
of the capsule should be recorded.

IMPORTANT PALPATION
FINDINGS

Condyle tenderness
which is equal to or greater than 2 on a 0 to 3 scale and which is more
pronounced than ipsilateral anterior temporalis and superficial masseter
tenderness indicates temporomandibular joint capsulitis. Patients with
this finding are very likely to express TMD symptoms which are driven
by temporomandibular joint-specific inflammation and/or mechanical deformation.

Tenderness of
the belly of the sternocleidomastoideus and/or upper trapezius may be
produced by inflammation of the temporomandibular joints. This can be
unilateral, bilateral or ipsilateral to the involved joint. These muscles
are almost always hypertonic as well as tender if temporomandibular
joint inflammation is the driving force behind this finding. This indicates
that this is not just referred pain, but a muscular reaction to heightened
neurologic activity produced by joint inflammation. This has been confirmed
by retrospective surgical testing (70,105) and anesthetic injection
studies (17, 105).

Temporomandibular
joint inflammation produces substantial hypertonicity and tenderness
of the paracervical musculature especially in the suboccipital region.
It may also cause hyper-contraction and tenderness of the scalene muscles
with associated pain and paresthesia in the upper extremities.

Temporomandibular
joint inflammation does not usually cause isolated tenderness of the
spinous processes and interspinous spaces in the cervical region. This
helps to differentiate primary cervical injury/pathology from temporomandibular
joint-cervical affect.

The stylomandibular
ligaments and the temporal tendons at their coronoid attachments should
also be palpated. Referred pain from the coronoid attachment includes
the eye, bridge of the nose, temporomandibular joint and ear (101).
Stylomandibular ligament inflammation refers pain to the preauricular
region, ear, neck and head (101).

The mastoid processes
are useful control areas for palpation. Except for mastoiditis or a
direct blow to the area, this region is nontender in most all patients
(severe temporomandibular joint inflammation may produce slight tenderness
in a few patients). This area is above the sternocleidomastoideus insertion
and lateral to the upper trapezial insertion. This is an area of thinly
covered bone and, while not identical to the temporomandibular joint
condyle, is similar. It thus provides an ideal area for comparison of
palpation responses. The area should be palpated two to three times
during the examination with the same pressure (3-5 pounds of pressure
applied with the pad of the index finger). This allows the doctor to
check for consistency of response. This is a valuable screening test
for hypersensitivity, false complaint and malingering.

TMD PROVOCATION
TESTS (CHALLENGES)

History, range of
motion, tracking, auscultation and palpation will give you 95% of the
information you need to develop an accurate diagnostic impression. To
challenge this impression, provocation tests may be used. Keep in mind
that the goal of these tests is to provoke a response from the patient
when injured/damaged tissue is stressed. Thus, by definition these tests
will aggravate the pathology. Use them sparingly and with discrimination.
If these tests are used repeatedly, healing may be undermined. These tests
may be performed during the initial examination and should only be repeated
if the response to conservative care has been poor and a surgical referral
is being considered.

SPECIFIC PROVOCATIONS

RESISTED PROTRUSION/LATEROTRUSION.
To perform resisted protrusion, place your thumbs on the point of the
patient's chin and your other fingers on the sides of the mandible for
stability. Have the patient push the mandible forward with a force equal
to your resistance. No joint movement should occur. If pain is produced,
the inferior head of the external (lateral) pterygoid muscle is implicated.
The pain will occur on the side of the involved muscle and may radiate
to the temporomandibular joint, ear and/or cheek. This muscle does attach
to the joint capsule and condyle and may stimulate true arthrogenous
symptoms. Any headache or neck pain produced should lead one to suspect
joint involvement. The internal (medial) pterygoids are also activated
during this test, although to a lesser extent. The pain pattern is very
similar to the external pterygoids, although pain is frequently felt
at the angle of the mandible as well.

By moving the thumbs slightly to the side of the chin and having the
patient push the mandible against the thumbs, each lateral pterygoid
(inferior head) can be tested for strength and/or isolated for involvement
in pain production. When performing these tests be careful that the
patient does not push the head forward as this win involve the cervical
region and confound the results.

PASSIVE MANDIBULAR
DISTALIZATION. The goal of this test is to press the condyles to the
back and/or superior aspects of the fossae. If there is inflammation
in the retrodiscal tissue or the superior/posterior articular surfaces,
pain may be elicited. If this test is positive, severe inflammation
of this region is indicated. Pain may be local to the involved joint
and/or referred to the head, ear, neck and shoulders. This test has
two limitations. First, inflammation may be predominantly in other areas
of the joint and secondly, the external pterygoid inferior head may
splint and prevent true compression despite the patient's attempt to
relax and allow you to press the condyles back into the fossae. As a
result, there may be substantial joint inflammation even when this test
is negative. There are two popular techniques for performing this test:

A. The doctor
faces the patient while the patient is either seated or supine. The
doctor places his or her thumbs on the point of the chin and the second
and third digits of each hand on the sides of the jaw. The doctor then
places the fourth and fifth digits of each hand under the angles of
the mandible. The patient pushes the mandible slightly forward against
resistance and then relaxes. While the mandible is relaxed have the
patient open their mouth approximately one-third of the way. Slowly
push back on the chin while lifting up under the angles of the mandible
as the patient keeps the jaw relaxed. The doctor alternates from straight
anterior/posterior pressure to pressure toward one joint and then the
other. During this procedure you may notice that the patient's muscles,
specifically the inferior heads of the external pterygoids, may resist
your attempt at distalization. To adjust for this, have the patient
repeat protrusion while you resist the attempt and then as the patient
relaxes per your instructions once again distalize the mandible and
press upward into the fossae.

B. The doctor
stands behind the seated patient and interlaces his or her fingers cupping
them under the patient's chin. The patient rests the back of their head
against the doctor's torso if a standard chair is used or against the
headrest of a dental chair if one is available. The patient then relaxes
and opens the mouth approximately one-third of the way. The doctor then
slowly pulls up and back pressing the condyles into the joint. The doctor
has great mechanical advantage during this technique and must be careful
not to injure the patient.

Local jaw
pain and/or referred pain, especially to the ears, suboccipital region,
neck and shoulders, signals a positive result for this test. A positive
result on this test, especially when resisted protrusion was negative,
is a strong indication of substantial temporomandibular joint inflammation
most likely in the posterior and superior aspects of the involved joints.

JOINT LOADING
DURING PROTRUSION. This technique is used to test for inflammation in
the anterior aspect of the temporomandibular joints (condyle against
posterior slope of the eminence with or without disc intervening). To
set up for this test stand behind the seated patient. If the patient
is seated in a dental chair, they can place the back of their head into
the headrest of the chair. If the patient is seated in a standard chair,
the test is best performed by having the patient rest their head against
your torso. Place your hands underneath the body of the mandible from
the mid body back to the angles and lift up gently, bringing the condyles
to the upper portion of the joints. Instruct the patient to separate
the teeth only slightly and then protrude the mandible. This should
occur without the teeth touching. Stop immediately if pain is produced
or joint locking occurs. This is a particularly threatening test and
should be performed with caution. Prior to performing the test instruct
the patient to stop any attempted protrusion at the first sign of pain
and/or locking. This way, any possibility of aggravating the condition
may be minimized.

Pain in the involved joint and/or pain referred to the ears, head, neck
or shoulders signals positive result. Other positive findings include
increased volume of clicking or frank locking as the condyle catches
behind an anterior adhesively restricted disc. Pain and locking together
during this test signals a disorder with a guarded prognosis for conservative
resolution.

DISTRACTION OF
THE TEMPOROMANDIBULAR JOINTS. This test may be performed with the patient
seated or supine. Some doctors perform this test one joint at a time
and others use a bilateral technique.

Bilateral supine technique: Have the patient lie supine and position
your body to face cephalad. Have the patient open his/her mouth and
then lean forward placing your thumbs over the mandibular teeth. Grasp
the undersurface of the mandible with the remaining fingers of both
hands. Having grasped the mandible firmly press down with the thumbs
effectively pulling the condyles away from the superior portion of the
fossae. Pre-instruct the patient to point to any areas of pain that
may occur as you perform the test. This technique stretches the muscles
as well as distracts the joints. Thus, the patient may point to any
number of areas. Pain in the joints is indicative of temporomandibular
joint inflammation (capsular and/or inflamed intra-articular scarification).
Pain in the masticatory muscles may indicate a myofascial problem such
as a trigger point, although masticatory muscle contraction secondary
to temporomandibular joint inflammation may produce the same result.
The most common positive finding for temporomandibular joint inflammation,
however, is local temporomandibular joint pain. A positive finding for
joint inflammation should discourage any temporomandibular joint manipulation
until the acute phase is controlled.

CLENCH ON SEPARATORS.
Clenching the teeth together (when a full complement of teeth is present
or missing teeth have been effectively replaced) for a few seconds upon
command should not cause the patient pain. Pain produced may be odontogenic
(including the periodontal ligament), muscular or arthrogenous. Suspected
tooth pain can be investigated by having the patient place cold and/or
hot liquids in the mouth as well as by percussion of the teeth as positive
findings on these tests tend to be indicative of odontogenic problems.
If the examining doctor is not a dentist, referral for a complete dental
exam is recommended. Non-dental pain may be myogenous or arthrogenous.
Differential diagnosis between muscular pain and the pain of joint inflammation
is aided by having the patient clench and/or chew on separators (items
placed between the upper and lower teeth). Some doctors use soft wax
for this, however cotton rolls will suffice. Pain produced when the
patient bites down on cotton rolls which have been placed between the
teeth bilaterally is most frequently of muscular origin. Joint inflammation
may be implicated in certain cases, however. This may be due to the
effect of joint inflammation on the muscle tissue reflexively. When
separators are placed unilaterally, the mechanics and interpretation
of the test are more complex. This test can be described by example.
If the cotton roll is placed between the upper and lower teeth on the
right and the patient has pain with biting down the following guidelines
apply: Ipsilateral pain indicates probable myofascial component with
possible joint inflammation on the side of pain; contralateral pain,
especially pain in the temporomandibular joint or ear, strongly suggests
temporomandibular joint inflammation on the side of pain. This is because
unilateral biting onto an object (whether a bolus of food or cotton
roll) compresses the contralateral joint and not the ipsilateral joint
(4).

In summary, provocation
tests can help to clarify the diagnostic impression. As the tests are
provocations of potentially damaged tissues they should be performed carefully
and not repeated routinely. They should be used during reexamination only
if the case is not progressing satisfactorily and the diagnosis needs
to be challenged. These tests are indicators of diagnostic probability
and do not stand alone as definitive.

RADIOLOGY

Numerous radiographic
examinations are available for the temporomandibular joints. It is advised
here that any radiographic evaluation of the temporomandibular joints
be interpreted by a specialist in the field of TMD. The most frequently
ordered studies include tomograms, transcranials and the panelipse. These
films have specific uses and limitations and are ordered generally when
fracture and/or pathology is suspected or specific treatment regimens
demand information about anatomic or other joint characteristics. While
an in-depth presentation on radiology is beyond the scope of this chapter,
a few pertinent diagnostic correlations should be mentioned.

Specific diseases,
tumors and fracture aside, x-rays of the temporomandibular joints cannot
identify the presence, past history or predicted future course/development
of a temporomandibular disorder (26).

Alterations in
bone morphology (as observed on x-ray) may occur as a result of successful
remodeling of the temporomandibular joints (83). Alterations in condyle/fossa
shape should not be interpreted as indicating degeneration unless signs
and symptoms of a joint-specific disorder are present. Even then, the
x-ray findings may be incidental. This includes plain films, tomography,
transcranials and the panelipse.

Corrected positional
tomograms can be used to assess a predisposition to anterior disc position.
This references the tendency of the condyle to sit behind the disc during
maximum intercuspation if the condyle is seated in the posterior/ superior
aspect of the fossa. This information can be very useful in case management
of the patient with symptom expressive internal derangement. Medical
laminographs taken with the patient lying down cannot provide this information.

SPECIAL TESTS

Special tests are
generally ordered when it is necessary to confirm the diagnostic impression.
These tests all have specific uses and limitations. They are useful in
classifying the temporomandibular disorder rather than establishing the
presence or absence of a disorder. The following is an overview only.

MRI. The MRI
is generally used to gain information that may alter the course of applied
therapy when conservative treatment is not working or soft tissue pathology
is suspected. While this test is subject to interpretation flaws, qualified
research has demonstrated that this technology can accurately identify
static disc position (118). The MRI currently can only infer disc dynamics
during movement. Even kinematic MRI cannot demonstrate disc dynamics
as the views are staged and do not account for intracapsular forces
which may affect these dynamics. This can cause difficulties in case
management if disc position is overvalued relative to disc dynamics.
T2 weighted or spin echo images are used to test for joint effusion
(96, 118). While the identification of joint effusion is an important
finding indicative of swelling and inflammation, a negative T2 study
does not rule out inflammation.

ARTHROGRAM. During
this test contrast medium is injected into one or both joint spaces
(inferior/superior) under visualization. Transcranial or tomographic
images are then taken and movement may be recorded on video tape (cine-arthrogram).
The cine-arthrogram provides information about disc position and real
time disc dynamics. The uni-compartmental study is the gold standard
test for disc/retrodiscal perforation (107). This test is usually performed
when joint surgery is likely,however, some practitioners use arthrography
to document disc/condyle relationship during repositioning splint therapy.

OSSEOUS SCINTIGRAPHY
(BONE SCAN). This is an extremely sensitive test for osseous pathology.
Good clinical correlation is necessary for accurate interpretation of
results, although a high correlation with symptomatic internal derangement
diagnoses has been reported (73). While positive findings in uncomplicated
trauma cases have been useful in identifying surgical candidates, this
test cannot stand alone in this regard. Negative studies do not rule
out the presence of inflammation. Imaging can be performed with a planar
camera or SPECT (single photon emission computerized tomography) imaging.
SPECT is the imaging of choice for the temporomandibular joints (73).

ANESTHETIC INJECTIONS.
Anesthetic injections of the temporomandibular joints as well as of
muscles, ligaments, nerves and tendons of the temporomandibular joint
apparatus are effective tools for investigating the relationship between
suspected pathology and expressed symptoms (77). One excellent example
is the potential relationship between an inflamed temporomandibular
joint and concurrent neck pain. In a retrospective review comparing
surgical results with the impact of pre-surgical intracapsular temporomandibular
joint Marcaine injections, the injection accurately predicted specific
areas of symptom relief in 94% of the cases (105).

CT SCAN. The temporomandibular
joint CT scan has decreased in popularity with the advent of MR imaging.
It is most frequently used to identify bony pathology and fractures.

DIAGNOSTIC CONFIRMATION
OF TMD

As the onset of a
TMD is not predictable, these disorders should be viewed as beginning
with the onset of symptoms. These symptoms may be local to, or occur at
some distance from, the involved tissue. If TMD is suspected, the first
order of business is to identify the location of the dysfunctional tissue
e.g. intracapsular versus extracapsular, as this will most clearly define
the immediate appropriate treatment plan. If both intracapsular and extracapsular
findings are present, one should try to ascertain which is more likely
to be driving the other. Consideration should then be given to the patient's
history with an eye to the most likely precipitating event as this will
profoundly influence the proper treatment and prognosis (e.g. chronic
insidious versus acute traumatic). Finally, any factors which may have
predisposed the patient to the onset of the disorder or threaten to perpetuate
its expression should be recorded. This, once again, is not unlike the
appropriate diagnostic workup for spinal, paraspinal and other musculoskeletal
disorders, although an expanded data basis specific to TMD is necessary.
For example, such issues as malocclusion, developmental oro-facial anomalies,
oro-facial parafunctional habits, sleep disorders and specific dental
health history will need be considered with TMD.

An appropriate clinical
diagnostic impression then should include symptoms expressed, location
of injured or dysfunctional tissue, potentially perpetuating factors and
probable etiology. These considerations are essential for intervention,
management and/or referral.

A SUMMARY OF SPECIFIC
DIAGNOSES

INTRACAPSULAR
DISORDERS

CAPSULITIS

Tenderness of
the condyle which is equal to or more prominent than tenderness of the
ipsilateral temporalis and superficial masseter musculature.

Temporomandibular
joint pain with mandibular distraction.

*Note: Pain with
resisted mouth closure or resisted protrusion may irritate capsulitis
and produce joint pain because the superior head of the external pterygoid
attaches to the capsule.

*Note: These last
two tests may stimulate inflamed retrodiscal tissue especially if the
disc is displaced anteriorly. This is sometimes termed retrodiscitis.
Synovitis is necessarily concurrent with retrodiscitis and there may be
little clinical value in distinguishing the two.

INTERNAL DERANGEMENT

Disc displacement
with reduction.
- Clicking in the temporomandibular joints during mouth opening and
protrusion.
- The mandible will deflect toward the disc until recapture.
- Medial/lateral displacement may produce clicking with laterotrusive
movements.

Disc displacement
without reduction (disc dislocation).
- Limited mouth opening usually at 26 - 32 mm.
- Limited protrusion usually at approximately 6 mm.
- If unilateral, the mandible will deviate to that side with opening
and protrusion (more pronounced upon protrusion).
- Medial
dislocation will limit mandibular movement to the opposite side.

HYPERMOBILITY

Audible, visible
and/or palpable movement of the condyle(s) past the temporal eminence.
If unilateral, the condition may be secondary to contralateral joint hypomobility.

*Joint dislocation
represents a combination of joint hypermobility and elevator muscle spasm.
The patient presents with exaggerated mouth opening and mandible protruded.
The condition may self-reduce or dislocation may be non-reducing. Reduction
is best accomplished with manipulation under anesthesia to minimize joint
damage.

ANKYLOSIS

If unilateral
there will be an unyielding restriction of opening and protrusion as
well as laterotrusion to the opposite side. Deviation will be toward
the involved side. If bilateral, all mandibular movements are markedly
restricted. While pain may be present, it is not the limiting factor
and restrictions are even less clinically modifiable by conservative
measures than with disc dislocation.

Ankylosis may
be bony or fibrous. Bony ankylosis will have positive radiographic findings
while fibrous ankylosis can only be inferred by lack of condylar movements.

DISC/RETRODISCAL
PERFORATION

Crepitus upon
auscultation.

May or may not
be associated with other signs of internal derangement and/or inflammation.

Spread of contrast
medium from inferior to superior joint space will be noted during unicompartmental
arthrography.

EXTRACAPSULAR DISORDERS

MASTICATORY MYOFASCITIS
(MYALGIA, M.P.D.)

Tender points
and/or trigger points found in involved muscles.

Patients present
with cyclic local, dull, aching pain.

May be a primary
diagnosis or secondary to other processes e.g. central nervous system
sensitization secondary to temporomandibular joint and/or upper cervical
facet inflammation.

As a primary process
masticatory myofascitis does not limit range of motion.

MYOSITIS

Tenderness over
entire muscle.

Acute onset of
continuous local pain with likely trauma or infectious etiology.

Muscle will be
swollen and warm to touch.

Pain-mediated
limited range of motion specific to involved muscle(s).

MYOSPASM

Acute onset of
continuous pain during spasm.

Sustained muscle
contraction even at rest.

No swelling of
muscle.

Pain-mediated
limited range of motion specific to involved muscle(s).

MUSCLE SPLINTING

Limited range
of motion specific to protected region.

Pain with movement
with little or no pain at rest (protected region may ache at rest).

Temporary relief
of local and/or referred pain with anesthetic injection.

SUMMARY

Temporomandibular
disorders are a subclassification of musculoskeletal disorders and produce
symptoms both local to the craniomandibular region and at some distance
from the area. Temporomandibular disorders are generally subclassified
as intracapsular and extracapsular and may be thought of as primary myofascial
disorders and inflammatory or mechanical disorders of joints, ligaments,
tendons and muscles. Symptom complexes vary greatly and frequently represent
the reflexive influence of craniomandibular pathology on the central nervous
system. Central nervous system sensitization and altered neuroplasticity
may result in a spread of neural activity throughout the triggering-cervical
complex. Reactive muscle contraction and associated trigger point expression
may produce pain and other symptoms throughout the head, neck, upper back
and upper extremities.

Accurate diagnosis
of the patho-etiology behind the production of TMD symptoms will result
in improved treatment results. Early identification of arthrogenous disorders
coupled with more accurate delivery of therapy may serve to prevent the
progression of temporomandibular joint degradation and stem the development
of resultant chronic pain presentations.